Portal vein thrombosis following laparoscopic splenectomy for beta-thalassemia: a case study.
ABSTRACT Portal vein thrombosis is a rare but well-recognized complication of splenectomy. We present the case of a 31-year-old woman with transfusion-dependent b-thalassemia who underwent a laparoscopic splenectomy to reduce her transfusion requirements. Postoperatively, she developed portal vein thrombosis, diagnosed by abdominal CT scanning on postoperative day 4. After being treated with anticoagulation and antibiotic therapy, she obtained prompt resolution of her symptoms. This report summarizes the first reported incidence of portal vein thrombosis following laparoscopic splenectomy and presents the current theories regarding the etiology and treatment of postsplenectomy portal vein thrombosis.
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ABSTRACT: The occurrence of thrombosis in the portal system is an underappreciated complication of splenectomy. Presenting symptoms are usually mild and nonspecific. The short hospital stay associated with the laparoscopic approach could delay the early diagnosis of this condition unless routine imaging controls are planned after discharge. The records of 40 patients who underwent laparoscopic splenectomy at our institution were reviewed for clinical signs of thrombosis in the portal system and associated factors. All patients were also enrolled in a color Doppler ultrasound surveillance program. Nine patients (22.5%) developed thrombosis of the splenic vein, progressing to the portal vein in five cases (12.5%). Six patients (15%) were symptomatic. Thrombosis occurred even as late as 4 months after splenectomy. Spleen weight was the only significant factor predictive of postoperative thrombosis. The combination of splenomegaly and an elevated preoperative platelet count was associated with a 75% incidence of this complication. The high risk of thrombosis after the laparoscopic resection of large spleens should prompt strict postoperative imaging surveillance, combined with a more aggressive anticoagulation prophylaxis.Surgical Endoscopy 08/2004; 18(7):1140-3. · 3.43 Impact Factor
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ABSTRACT: Portal vein thrombosis (PVT) is an uncommon cause for presinusoidal portal hypertension. PVT can be caused by one of three broad mechanisms: (1) spontaneous thrombosis when thrombosis develops in the absence of mechanical obstruction, usually in the presence of inherited or acquired hypercoagulable states; (2) intrinsic mechanical obstruction because of vascular injury and scarring or invasion by an intrahepatic or adjacent tumor; or (3) extrinsic constriction by adjacent tumor, lymphadenopathy or inflammatory process. Usually, several combined factors are necessary to result in PVT. The consequences of portal vein thrombosis are mostly related to the extension of the clot within the vein. Gastrointestinal bleeding from gastroesophageal varices is the most frequent presentation. Noninvasive imaging techniques are currently used for the screening of patients and the initial diagnosis of PVT. The invasive techniques are reserved for cases when noninvasive techniques are inconclusive, before percutaneous interventional treatment, or in preoperative assessment of patients who are candidates for surgery. Recanalization of the portal vein with anticoagulation alone may not be consistent or appropriate in highly symptomatic patients. Catheterization of the superior mesenteric artery (SMA) is helpful for diagnosis as well as for therapy by allowing the intra-arterial infusion of thrombolytic drugs in the same setting. Direct transhepatic portography allows precise determination of the degree of stenosis and extension within the portal vein, as well as pressure measurements. Thrombotic occlusions of the portal, mesenteric, and splenic veins can be managed by mechanical thrombectomy (MT) or pharmacologic thrombolysis. Underlying occlusions because of organized or refractory thrombus or fixed venous stenosis are best corrected by balloon angioplasty and stent placement. Access into the portal venous system can also be established through creating a transjugular intrahepatic portosystemic shunt (TIPS). Creating a TIPS is also important in the setting of PVT associated with cirrhosis to decompress portal hypertension and improve portal venous flow. PVT involving the portal, splenic, and/or mesenteric veins can also complicate a preexisting TIPS in which case the shunt can be readily used as therapy access. Several techniques may be used to recanalize the shunt and portal venous system, including thrombolytic therapy, balloon angioplasty/embolectomy, suction embolectomy, basket extraction of clots, and mechanical thrombectomy with a variety of devices. Advantages of MT include the potential to rapidly remove thrombus without the need for prolonged thrombolytic infusions, and reducing the potential life-threatening complications of thrombolytic therapy. Possible drawbacks include the risk of intimal or vascular trauma to the portal vein, which may promote recurrent thrombosis.Techniques in Vascular and Interventional Radiology 04/2003; 6(1):59-69.
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ABSTRACT: A hypercoagulable state has been documented in patients with β-thalassemia. It could result in thromboembolic events in several organs including brain involvement, which deserves particular attention. We summarized the prevalence of cerebral involvement in patients with β-thalassemia worldwide. We conducted an electronic search on PUBMED (MEDLINE), SCOPUS, and Google Scholar databases up to January 2011. Overall 152 thalassemic patients with cerebral thromboembolic events and a proportion of 1.13% (134 of 11770) were recorded. From all patients with cerebral thromboembolic events, 74 (48%) were splenectomized. Cerebral thromboembolic events were reported after transfusion in six β-thalassemia major, and two β-thalassemia intermedia patients. Three β-thalassemia major patients had irregular transfusion and 22 β-thalassemia intermedia patients were not transfused. Thrombocytosis were determined in 11 β-thalassemia major, and 15 β-thalassemia intermedia patients. Cardiomyopathy was present in 13 β-thalassemia major and four β-thalassemia intermedia patients. Also, nine β-thalassemia major patients had diabetes. Activated protein C resistant, decreased protein C or protein S or plasminogen level was detected in eight β-thalassemia major patients. Cerebral involvement appears to be associated with increasing age, transfusion naivety, splenectomy, thrombocytosis, intensive transfusion, decreased protein C level, and having risk factors for cerebrovascular accident such as cardiomyopathy, and diabetes. In light of these findings, diagnostic MRI is recommended in high-risk groups to screen for early asymptomatic brain damage. If brain ischemia is found, the administration of antiplatelet aggregants or blood transfusion is likely to be beneficial. In addition, in thalassemic patients who complicated with a thromboembolic event, secondary prophylaxis could be helpful to prevent cerebral thromboembolic events.Blood coagulation & fibrinolysis: an international journal in haemostasis and thrombosis 02/2012; 23(3):212-7. · 1.25 Impact Factor